Excitability of canine colon circular muscle disconnected from the network of interstitial cells of Cajal Journal Articles uri icon

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abstract

  • The 6 cpm omnipresent slow waves recorded in the circular muscle (CM) layer of canine colon are generated at the submucosal surface of the CM layer. After removal of the submucosal network of interstitial cells of Cajal (ICC), 66% of the CM preparations (25 of 38) were quiescent in Krebs solution. In the presence of carbachol, seven of nine of these spontaneously quiescent CM preparations demonstrated slow wave-like activity with mean frequency, duration and amplitude of 5.9 ± 0.4 cpm, 2.8 ± 0.5 s, and 0.8 ± 0.2 mV, respectively. Similar slow wave-like activities were induced by TEA (seven out of eight quiescent CM preparations) with frequency, duration and amplitude of 6.1 ± 0.2 cpm, 2.7 ± 0.5 s, and 1.0 ± 0.2 mV, respectively, and by BaCl2 (eight of eight quiescent CM preparations) with frequency, duration, and amplitude of 6.3 ± 0.3 cpm, 1.8 ± 0.2 s, and 0.5 ± 0.1 mV, respectively. All the induced activities were abolished in the presence of 1 μM D600. CM preparations with the submucosal ICC network intact (ICC–CM) showed slow wave activity in Krebs solution at a frequency of 6.2 ± 0.2 cpm, a duration of 3.6 ± 0.2 s, and an amplitude of 1.0 ± 0.1 mV (n = 22). When ICC–CM preparations were stimulated by BaCl2, carbachol, or TEA, the slow wave frequency did not change significantly, but the duration increased as well as the amplitude. In the presence of D600, the upstroke of slow waves remained and the frequency was not affected. The ability to generate slow wave-like activity after potassium conductance blockade in spontaneously quiescent CM disconnected from the ICC network suggested that circular muscle cells have ionic mechanisms for intrinsic oscillatory activity and are capable of actively participating in the conduction and generation of slow waves.Key words: colon, smooth muscle, interstitial cells of Cajal, canine, slow waves, excitability.

publication date

  • February 1, 1992